6AN (6-Aminonicotinamide)

Catalog No.S9783 Batch:S978302

Technical Data

Formula	C₆H₇N₃O
Molecular Weight	137.14	CAS No.	329-89-5
Solubility (25°C)*	In vitro	DMSO	27 mg/mL (196.87 mM)
		Water	Insoluble
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description

6AN (6-Aminonicotinamide) is an antimetabolite used to inhibit the NADPH-producing pentose phosphate pathway (PPP) in many cellular systems, making them more susceptible to oxidative stress. 6-Aminonicotinamide is a competitive inhibitor of NADP+-dependent enzyme glucose-6-phosphate dehydrogenase (G6PD) with Ki of 0.46 μM.

Targets

G6PD ^[1]
(Cell-free assay)

0.46 μM(Ki)

In vitro

Blocking the pentose phosphate pathway (PPP) by 6-AN significantly inhibits mES colony formation in the presence of a normal concentration of glucose. 6-AN treatment effectively inhibits AKT phosphorylation and activation of its downstream effector S6. 6-AN treatment has no effect on the ERK and PDK1 activities, suggesting an AKT-specific effect. 6-AN treatment inhibits cell growth.^[2]

In vivo

PTEN null human cancer cells and in vivo murine models are sensitive to 6-AN (anti-PPP, anti pentose phosphate pathway) treatments, suggesting the importance of the PPP in maintaining AKT activation even in the presence of a constitutively activated PI3K pathway. The treatment of TALL models with 6-AN significantly increases the Phlda3 mRNA and protein levels, accompanied by substantial decreases in the levels of P-AKT and P-S6 as well as the PPP metabolic intermediates.^[2]

Protocol (from reference)

Cell Assay:^{^[2]}	Cell lines HeLa cells, mES cells Concentrations 100 nM Incubation Time 24 h, 2 days, 3 days, 4 days Method PHLDA3 knockout blocks the effects of 6-AN, R5P or uridine on cell growth in vitro. Isogenic PHLDA3 WT and knockout HeLa cells are seeded in 96-well plates at a density of 1000 cells/well. After 48 h, the cells are treated with 6-AN (100 nM). Cell viability is detected by CCK-8 assays at indicated time points.
Animal Study:^{^[2]}	Animal Models male CAnN.Cg-Foxn1nu/CrlVr mice Dosages 1 mg/kg, 15 mg/kg Administration IP

Cell Assay:^{^[2]}

Cell lines
HeLa cells, mES cells
Concentrations
100 nM
Incubation Time
24 h, 2 days, 3 days, 4 days
Method
PHLDA3 knockout blocks the effects of 6-AN, R5P or uridine on cell growth in vitro. Isogenic PHLDA3 WT and knockout HeLa cells are seeded in 96-well plates at a density of 1000 cells/well. After 48 h, the cells are treated with 6-AN (100 nM). Cell viability is detected by CCK-8 assays at indicated time points.

Animal Study:^{^[2]}

Animal Models
male CAnN.Cg-Foxn1nu/CrlVr mice
Dosages
1 mg/kg, 15 mg/kg
Administration
IP

References

Selleck's 6AN (6-Aminonicotinamide) has been cited by 9 publications

Metabolic classification suggests the GLUT1/ALDOB/G6PD axis as a therapeutic target in chemotherapy-resistant pancreatic cancer [ Cell Rep Med, 2023, S2666-3791(23)00315-4]	PubMed: 37597521
Metabolic classification suggests the GLUT1/ALDOB/G6PD axis as a therapeutic target in chemotherapy-resistant pancreatic cancer [ Cell Rep Med, 2023, 4(9):101162]	PubMed: 37597521
PI3K/mTOR inhibitors promote G6PD autophagic degradation and exacerbate oxidative stress damage to radiosensitize small cell lung cancer [ Cell Death Dis, 2023, 14(10):652]	PubMed: 37802999
PI3K/mTOR inhibitors promote G6PD autophagic degradation and exacerbate oxidative stress damage to radiosensitize small cell lung cancer [ Cell Death Dis, 2023, 14(10):652]	PubMed: 37802999
Aberrant metabolite trafficking and fuel sensitivity in human pluripotent stem cell-derived islets [ Cell Rep, 2023, 42(8):112970]	PubMed: 37556323
Insulin-induced gene 2 protects against hepatic ischemia-reperfusion injury via metabolic remodeling [ J Transl Med, 2023, 21(1):739]	PubMed: 37858181
Insulin-induced gene 2 protects against hepatic ischemia-reperfusion injury via metabolic remodeling [ J Transl Med, 2023, 21(1):739]	PubMed: 37858181
Metabolic heterogeneity protects metastatic mucosal melanomas cells from ferroptosis [ Int J Mol Med, 2022, 50(4)124]	PubMed: 36004461
Metabolic plasticity imparts erlotinib-resistance in pancreatic cancer by upregulating glucose-6-phosphate dehydrogenase [ Cancer Metab, 2020, 8:19]	PubMed: 32974013

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SHIPPING AND STORAGE
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